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Protection by borneol on cortical neurons against oxygen-glucose deprivation/reperfusion: involvement of anti-oxidation and anti-inflammation through nuclear transcription factor κappaB signaling pathway.
Neuroscience. 2011 Mar 10; 176:408-19.N

Abstract

Borneol, a terpene and bicyclic organic compound found in several species, can easily penetrate the blood-brain barrier (BBB) and helps the absorption of many agents through BBB in the brain, but there has been no study about its direct action on neurons in the CNS. In the present study, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD/R) to investigate the neuroprotective effects of borneol and the related mechanisms. We demonstrated that borneol reversed OGD/R-induced neuronal injury, nuclear condensation, intracellular reactive oxygen species (ROS) generation, and mitochondrial membrane potential dissipation. The elevation of nitric oxide (NO), the increase of inducible nitric oxide synthase (iNOS) enzymatic activity and the upregulation of iNOS expression were also attenuated by borneol. The inhibition of caspase-related apoptotic signaling pathway was consistently involved in the neuroprotection afforded by borneol. Meanwhile, borneol inhibited proinflammatory factor release and IκBα degradation, and blocked nuclear transcription factor κappaB (NF-κB) p65 nuclear translocation induced by OGD/R. On the other hand, borneol did not show obvious effect on the inhibition of phospho-IKKα activation. Furthermore, it failed to affect the OGD/R-induced enhanced level of phospho-SAPK/JNK. In conclusion, our study indicated that borneol protects against cerebral ischemia/reperfusion injury through multifunctional cytoprotective pathways. The mechanisms of this reversal from OGD/R may be involved in the alleviation of intracellular ROS and iNOS/NO pathway, inhibition of inflammatory factor release and depression of caspase-related apoptosis. Among these effects, the inhibition of IκBα-NF-κB and translocation signaling pathway might play a significant role in the neuroprotection of borneol.

Authors+Show Affiliations

National Center for Pharmaceutical Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21168474

Citation

Liu, R, et al. "Protection By Borneol On Cortical Neurons Against Oxygen-glucose Deprivation/reperfusion: Involvement of Anti-oxidation and Anti-inflammation Through Nuclear Transcription Factor κappaB Signaling Pathway." Neuroscience, vol. 176, 2011, pp. 408-19.
Liu R, Zhang L, Lan X, et al. Protection by borneol on cortical neurons against oxygen-glucose deprivation/reperfusion: involvement of anti-oxidation and anti-inflammation through nuclear transcription factor κappaB signaling pathway. Neuroscience. 2011;176:408-19.
Liu, R., Zhang, L., Lan, X., Li, L., Zhang, T. T., Sun, J. H., & Du, G. H. (2011). Protection by borneol on cortical neurons against oxygen-glucose deprivation/reperfusion: involvement of anti-oxidation and anti-inflammation through nuclear transcription factor κappaB signaling pathway. Neuroscience, 176, 408-19. https://doi.org/10.1016/j.neuroscience.2010.11.029
Liu R, et al. Protection By Borneol On Cortical Neurons Against Oxygen-glucose Deprivation/reperfusion: Involvement of Anti-oxidation and Anti-inflammation Through Nuclear Transcription Factor κappaB Signaling Pathway. Neuroscience. 2011 Mar 10;176:408-19. PubMed PMID: 21168474.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protection by borneol on cortical neurons against oxygen-glucose deprivation/reperfusion: involvement of anti-oxidation and anti-inflammation through nuclear transcription factor κappaB signaling pathway. AU - Liu,R, AU - Zhang,L, AU - Lan,X, AU - Li,L, AU - Zhang,T-T, AU - Sun,J-H, AU - Du,G-H, Y1 - 2010/12/16/ PY - 2010/09/19/received PY - 2010/10/28/revised PY - 2010/11/13/accepted PY - 2010/12/21/entrez PY - 2010/12/21/pubmed PY - 2011/6/2/medline SP - 408 EP - 19 JF - Neuroscience JO - Neuroscience VL - 176 N2 - Borneol, a terpene and bicyclic organic compound found in several species, can easily penetrate the blood-brain barrier (BBB) and helps the absorption of many agents through BBB in the brain, but there has been no study about its direct action on neurons in the CNS. In the present study, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD/R) to investigate the neuroprotective effects of borneol and the related mechanisms. We demonstrated that borneol reversed OGD/R-induced neuronal injury, nuclear condensation, intracellular reactive oxygen species (ROS) generation, and mitochondrial membrane potential dissipation. The elevation of nitric oxide (NO), the increase of inducible nitric oxide synthase (iNOS) enzymatic activity and the upregulation of iNOS expression were also attenuated by borneol. The inhibition of caspase-related apoptotic signaling pathway was consistently involved in the neuroprotection afforded by borneol. Meanwhile, borneol inhibited proinflammatory factor release and IκBα degradation, and blocked nuclear transcription factor κappaB (NF-κB) p65 nuclear translocation induced by OGD/R. On the other hand, borneol did not show obvious effect on the inhibition of phospho-IKKα activation. Furthermore, it failed to affect the OGD/R-induced enhanced level of phospho-SAPK/JNK. In conclusion, our study indicated that borneol protects against cerebral ischemia/reperfusion injury through multifunctional cytoprotective pathways. The mechanisms of this reversal from OGD/R may be involved in the alleviation of intracellular ROS and iNOS/NO pathway, inhibition of inflammatory factor release and depression of caspase-related apoptosis. Among these effects, the inhibition of IκBα-NF-κB and translocation signaling pathway might play a significant role in the neuroprotection of borneol. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/21168474/Protection_by_borneol_on_cortical_neurons_against_oxygen_glucose_deprivation/reperfusion:_involvement_of_anti_oxidation_and_anti_inflammation_through_nuclear_transcription_factor_κappaB_signaling_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(10)01520-4 DB - PRIME DP - Unbound Medicine ER -